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DM SEMINAR
Invasive and non-invasive hemodynamic monitoring in
the ICU
Dr. SACHIN KUMAR 14.03.08
Not everything that counts can becounted; And not everything that can be countedcounts
ALBERT EINSTEIN
INTRODUCTION • Hemodynamic monitoring - cornerstone in
the management of the critically ill patient
• Identify impending cardiovascular insufficiency, its probable cause, and response to therapy
• Despite the many options available, utility of most hemodynamic monitoring is unproven.
Intensive Care Med. 2008 Jan 5 .e pub
Why hemodynamic monitoring?
• Physicians have developed a psychological dependence on feedback from continuous hemodynamic monitoring tools, independent of their utility
• Effectiveness of hemodynamic monitoring to improve outcome limited to specific patient groups and disease processes for which proven effective treatments exist
Chest. 2007;132(6):2020-9
Rationale for Hemodynamic Monitoring
• Monitoring device will improve patient-centered outcomes when coupled to a treatment which, itself, improves outcome
• Time - crucial for early diagnosis of hemodynamic catastrophe - earlier therapy improves outcome in this situation
. N Engl J Med 2001; 345:1368–1377
Hemodynamic Monitoring
Non Invasive • Clinical variables • BP • ECG• Echocardiography • Esophageal doppler • Gastric tonometry
Invasive • CVP• PAOP • Pulse waveform
analysis • Microcirculation
– SvO2/ ScvO2– DO2/VO2– Lactate levels
CLINICAL PARAMETERS
• Blood pressure• Heart rate and
rhythm• Rate of capillary
refill of skin after blanching
• Urine output• Mental status • Effects of body
position on blood pressure Level 1 D
Intensive Care Med. 2007; 33:575–590International Consensus Conference
BLOOD PRESSURE • Arterial pressure is commonly measured non
invasively on an intermittent basis using a sphygmomanometer
• Normal blood pressure ≠ hemodynamic stability
• Hypotension (MAP < 65 mmHg) is always pathological
• No RCTs evaluating the impact of arterial pressure monitoring on outcomes when used in ICU or operating room Intensive Care Med. 2008
Jan 5 .e pub
Critical Care 2005, 9:566-572
Measuring Blood Pressure • Mercury sphygmomanometer• Oscillatory method
• Measures mean pressure - systolic and diastolic pressures are calculated, prone to error
• Infra sound / Ultrasonic technology • Very low frequency components of Krotokoff sounds below 50 Hz-
very operator dependent
• Impedance plethysmography • Monitors change in electrical impedance with local pulsatile arterial
distension occurring with each cardiac cycle
• Arterial tonometry• Applied pressure measured by sensors and arterial waveform
constructed using an algorithm- not shown good correlation with directly measured pressure Crit Care Clin.2007; 23 :383–400
INVASIVE BP• Guidelines recommend invasive blood pressure
measurement in refractory shock - Level 1D
• Intra-arterial pressure measurement more precise
• Continuous monitoring of pressure
• Blood sampling for blood gas analysis
• Pulse waveform analysis - beat-to-beat waveform analysis - CO can be determined continuously
Intensive Care Med. 2007; 33:575–590International Consensus Conference
What is the target BP ?• No threshold BP that defines adequate
organ perfusion among organs, between patients, or in same patient over time
• Based mainly on anecdotal experience, a systolic pressure of 100mmHg usual target, with HR < 120 B/min- Controversial
• MAP ≥ 65 mmHg - Initial target in septic shock,>40 mmHg in hemorrhagic shock and > 90 mmHg in Traumatic brain injury –Level 1 B
Curr Opin Crit Care.2001; 7:422–430
Intensive Care Med. 2007; 33:575–590International Consensus ConferenceSurviving sepsis Campaign 2008
Arterial waveform Analysis
• PiCCO (Pulsion Medical Systems) uses the aortic transpulmonary thermodilution curve to calculate CO
• LiDCO injection dilution method using Lithium as contrast : good correlation with thermodilution
• A large PP/SV variation (10% to 15%) is indicative of hypovolemia and predictive of volume responsiveness
Crit Care Med.2003; 31:793–99
Crit Care Clin.2007; 23 :383–400
ECG IN ICU
• Arrhythmia Monitoring – Up to 95% of AMI have arrhythmia within 1st 48
hrs – Up to 1/3 have VT. Early diagnosis and prompt
treatment may improve survival – Heart rate variability may reflect prognosis
• Ischemia Monitoring – Significant uncertainty to reliably detect
myocardial ischemia and diagnose MI in critically ill patients Crit Care Med 2006; 34:1338–1343
Technical issues • Patient safety requirements
– Proper grounding of equipment – Insulation of exposed lead connectors
• Adequate signal size – Good site preparation– Electrodes – Conducting gel – Appropriate signal damping
• Personnel issues – Formal training of ICU staff– Physician / cardiology back up
Evidence • Ischemia in ICU related to pain, fluid balance,
fever, catecholamine levels, or other physical stresses
• Hurford et al - worsening of ischemia (cont ECG ) in patients rapidly weaned from positive pressure to spontaneous ventilation
• Continuous ECG monitoring in ICU detected a 6.4% incidence of ischemia during weaning
• Patients with ischemia fail to wean more commonly Chest 1996;109;1421-1422
Echocardiography in ICU • Sole imaging modality that provides real-time
information on cardiac anatomy and function at bedside
• Ideally suited to early hemodynamic evaluation of patients with persistent shock despite aggressive goal-directed therapy
• European survey - only 20% of intensivists have certification in echocardiography
Intensive Care Med 2002 (Suppl) 28(1):S18 - 13.
Ann Emerg Med.2006 48:28–54
INDICATIONS – TTE IN ICU
- Hemodynamic instability– Ventricular failure– Hypovolemia– Pulmonary embolism– Acute valvular dysfunction– Cardiac tamponade
- Complications after cardiothoracic surgery- Infective endocarditis- Aortic dissection and rupture- Unexplained hypoxemia- Source of embolus
Crit Care Med 2007;35[Suppl.]:S235–S249
INDICATIONS – TEE IN ICU• High image quality vital
– Aortic dissection - Intracardiac thrombus– Assessment of endocarditis
• Inadequately seen by TTE – Thoracic aorta - Left atrial appendage– Prosthetic valves
• Inadequate image clarity with TTE – Severe obesity– Emphysema
• Mechanical ventilation with high-level PEEP • Presence of surgical drains, surgical incisions,
dressings• Acute perioperative hemodynamic derangements
Ventricular Function• Left Ventricular Systolic Function
• Significant LV dysfunction is common in critically ill patients (26%)
• Important for guiding resuscitation and informing decisions management with unexplained hemodynamic instability
• Sepsis-Related Cardiomyopathy• Cause of hemodynamic instability (hypovolemic,
cardiogenic, or distributive origin)• Subsequent optimization of therapy (fluid administration,
inotropic or vasoconstrictor agent)• Repeat bedside examination vital in assessing the
adequacy and efficacy of therapy
Am J Cardiol 2003; 91:510–513
Right Ventricular Function andVentricular Interaction
• In critical care setting, massive pulmonary embolism (PE) and ARDS - two main causes of acute cor pulmonale in adults
• Regional RV dysfunction had a sensitivity of 77% and a specificity of 94% for diagnosis of acute PE; PPV - 71% and NPV - 96%
• RV dysfunction may alter therapy (fluid loading, vasopressors, thrombolytics) and provide information about prognosis
Crit Care Med 2001;29:1551–55
Assessment of Filling Pressuresand Volume Status
• A dilated IVC (diameter of 20 mm) without a normal inspiratory decrease in caliber (50% with gentle sniffing) usually indicates elevated RA pressure
• In MV pt. 12% cutoff value in IVC diameter variation - respond to a fluid challenge( CO > 15 %, with PPV and NPV of 93% and 92%, respectively
Intensive Care Med (2008) 34:243–249
Cardiac Tamponade in the ICU• Myocardial or coronary perforation secondary to
catheter-based interventions (pacemaker lead insertion, central catheter placement, or percutaneous coronary interventions)
• Uremic or infectious pericarditis• Compressive hematoma after cardiac surgery• Proximal ascending aortic dissection• Blunt or penetrating chest trauma• Complication of myocardial infarction (e.g., ventricular
rupture)• Pericardial involvement by metastatic disease or other
systemic processes
Bedside Echocardiography vs PAC in ICU
• TEE produced a change in therapy in at least one third of ICU patients, independent of the presence of a PAC
• Study by Benjamin et al. TEE was performed in 12 ± 7 mins vs. ≥ 30 mins for PAC insertion
• Bedside echocardiography has a better safety profile
• PAC continuous monitoring technique to assess the response to a therapeutic intervention
Chest 1995; 107:774–779
J Cardiothorac Vasc Anesth 1998; 12:10–15
Effect of ECHO in the diagnosis and management in ICU
• Changes in management after TEE in 30– 60% of patients leading to surgical interventions in 7–30%
• Critically ill patients with unexplained hypotension, new diagnoses were made in 28% - leading to surgical intervention in 20%
• ECHO for diagnosis in patients with clinical evidence of ventricular failure and persistent shock despite adequate fluid resuscitation - Level 2 B
Crit Care Med 2007; 35[Suppl.]:S235-49
J Am Coll Cardiol 1995; 26:152–15
Intensive Care Med. 2007; 33:575–590International Consensus Conference
ECHO – Final words • All physicians in charge of critically ill patients should be trained
in goal directed echocardiography• Far from being competitive or conflicting, use of
echocardiography by intensivists and cardiologists is complementary
• German Society of Anesthesiology and Intensive Care Medicine- already developed their own certification
• Brief (10 hrs) formal training in using a handheld ECHO system, intensivists able to successfully perform limited TTE in 94% of patients and interpreted correctly in 84% - changed management in 37% of patients.
• “ECHO-in-ICU group”- France 2004
Intensive Care Med .2008.34:243–249
EDM - Clinical Application• EDM useful for detecting changes that otherwise have
gone unnoticed - covert and overt compensated hypovolemia
• EDM shown to predict subsequent complications in the critically ill.
• EDM is as good or better than pulmonary artery pressures for indicating changes in preload
• A reduction in postoperative complications was reported, with a significant reduction in-hospital length of stay in 4 studies
Crit Care Med. 1999;27(1):A111.
N Engl J Med. 2001;345(19):1368-77.
Intensive Care Med.2008 .JAN 5 – E pub
Limitations – EDM
Esophageal Doppler monitoring contraindicated• pathology of the esophagus • coarctation of aorta• Intraaortic balloon pumps• Coagulopathies
Further RCT are needed to evaluate EDM inICU
Gastric Tonometry
• Gastric intramucosal pH and carbon dioxide tension - attractive option for diagnosis and monitoring of splanchnic hypoperfusion
• Prolonged acidosis in gastric mucosa - a sensitive, but not specific, predictor of outcome in critically ill patients
Curr Opin Crit Care 2001, 7:122-127
Current position
• Guidelines do not recommend routine use of gastric tonometry and capnography to assess regional or micro-circulation- Level 1B
• Gomersall et al. showed no clinically or statistically significant differences in ICU or hospital survival, organ function, or duration of stay
Crit Care Med.2000;28:607–614
Intensive Care Med (2007) 33:575–590International Consensus Conference
INVASIVE MONITORING
• Information received cannot be acquired from less invasive and less risky monitoring
• Information received improves the accuracy of diagnosis, prognosis, and/or treatment based on known physiological principles
• Changes in diagnosis and/or treatment result in improved patient outcome (morbidity and mortality)
Central venous pressure
• Central venous pressure very common clinical measurement, but frequently misunderstood and misused
• CVP can be obtained with transducers and electronic monitors, simple water manometer, by simply JVP on physical examination
• Assessment of volume status and preload of heart- Common indication
• Most readily obtainable target for fluid resuscitation
Surviving sepsis campaign.2008
Rationale for the use of central venouspressure
• CVP and CO determined by interaction of two function curves: cardiac function curve and return curve
Principles of measurementLeveling• Standard reference level for assessment
sternal angle, 5 cm vertically above the mid-point of the right atrium - even when the person sits up at a 60º angle
• In supine patient, reference level -intersection of the fourth intercostal space with midaxillary line (3 mm Hg / 4.2 cm > sternal angle measurement )
Am J Respir Crit Care Med 2004; 169:A344
Principles of measurementTransmural pressure• CVP, should be made at end expiration - pleural
pressure is closest to atmospheric pressure• intrinsic or extrinsic PEEP, pericardial fluid, or
increased abdominal pressure can increase CVP
• PEEP of 10 cmH2O, increases the measured CVP by less than 3 mmHg in normal lung and even less in deceased lung
Curr Opin Crit Care.2006;12:219–227.
Potential Uses of the CVP• CVP only elevated( > 10 mm Hg ) in disease,
but clinical utility of CVP as a guide to diagnosis or therapy has not been demonstrated
• If CVP is ≤ 10 mmHg then CO decrease when 10 cm H2O PEEP applied whereas a CVP above 10 mmHg - no predictive value
• Fluid resuscitation initially target a CVP of at least 8 mm Hg (12 mm Hg in mechanically ventilated patients)- Level 1 C
Critical Care 2005, 9:566-572
Surviving Sepsis Campaign.2008
Potential Uses of the CVP
• Using ECHO > 36% SVC collapse during positive-pressure inspiration or complete IVC collapse - CVP is below 10 mmHg.
• However no threshold value of CVP that identifies patients whose CO will increase in response to fluid resuscitation
Intensive Care Med 2004;30:1734-1739
Crit Care Med 2004;32:691-699
PULMONARY ARTERY CATHETER
• 1970 PAC introduced• 1976 FDA charged with
insuring device safety & effectiveness
• Designated as Class IIrequiring special controls
• 1.5 million in US/yr– 30% cardiac surgery– 30% cardiac cath– 25% high risk surgery– 15% MICU
JAMA 2001, 286:348-350.
PAC based hemodynamic measurements
• The use of an indwelling catheter to measure
• – pulmonary artery pressure• – pulmonary capillary wedge pressure• – right atrial pressure• – pulmonary artery oxygen saturation• – thermodilution cardiac output
in the intensive care unit
ISSUES
• Do we have data to improve our definition of the type of patients or diseases for which PAC may improve quality of care and outcomes in the ICU?
• Can the data provided by the PAC improve outcomes in severely ill patients?
• Does PAC insertion carry a significant risk of complications?
Physician Knowledge of PAC
0102030405060708090
100
PGY1 2-3 4-6 Staff Expert
JAMA 264:2928,1990
PAC VS NO PAC
0
20
40
60
80
100
120
0 5 10 15 20 25 30
days
% a
live NO PAC
PAC
Connors, JAMA 276;889,1996
Why do we need PAC
• Hemodynamic profiles predicted in 56%• PAC derived profiles changed therapy in
50%• No change in over all mortality!• Improvement in mortality of Pts. With
shock not responding to usual measures
Mimoz et.al.CCM 1994;22:573-9
Evidence for EffectivenessDecompensated Heart Failure:
ESCAPE trial• Randomized trial of PAC vs. no PAC
– 433 pts hospitalized with CHF and volume overload– In PAC group: goal PCW 15 and RA 8– PAC group had greater wt loss (4.0 vs 3.2 kg) but similar final BUN/creat– 9 serious adverse events in PAC group (infection, bleed, catheter knot, VT, pulmonaryinfarction) ESCAPE Investigators. JAMA 2005; 294: 1625
Evidence for EffectivenessDecompensated Heart Failure:
ESCAPE trial• For the primary
endpoint, there wasno differencebetween interventionand control groups:
ESCAPE Investigators. JAMA 2005; 294: 1625
Evidence for EffectivenessMedical ICU: PAC-Man trial
• Randomized trial of PAC vs. no PAC– 1041 pts admitted to ICU who attending
thought needed a PAC. 66% medical. 65% multi-organ dysfunction.
– Therapy at the discretion of the clinician– Serious complications occurred in 10% of
pts in the PAC group
Harvey et al. Lancet 2005; 366: 472
Evidence for EffectivenessMedical ICU: PAC-Man trial
• For the primaryendpoint, there wasno differencebetween interventionand control groups:
Harvey et al. Lancet 2005; 366: 472
Evidence for EffectivenessMeta-analysis
• Quantitative review of 13 RCTs of PAC vs. no PAC in
– medical– surgical– cardiac patients• Significantly higher rate of use of vasodilator and
inotropic agents in PAC groups• No difference in mortality between groups
Shah et al. JAMA 2005; 294: 1664Critical Care 2006, 10(Suppl 3):S8
Evidence for EffectivenessMeta-analysis
• Use of PAC did not improve survival or decrease the length of hospital stay
• None of the studies used PAC derived variables to drive therapies of proven benefit
• Merely noted the impact of having a PAC in place on outcome.
Shah et al. JAMA 2005; 294: 1664Critical Care 2006, 10(Suppl 3):S8
NIH ARDS Net FACTT (Fluids and Catheters Treatment Trial)
• Multicenter trial to evaluate safety and efficacy of PAC-guided versus CVC-guided management in reducing mortality and morbidity in patients with established ALI
• Only trial coupling a treatment protocol with use of PAC
• compared a ‘fluid conservative’ approach with a ‘fluid liberal’ strategy with specific hemodynamic goals and treatment strategies
N Engl J Med 2006;354:2213-24.Critical Care 2008, 12:301
FACTT Protocol
Fluid boluses or diuretics are used to move hemodynamically stable patients toward filling pressure targets:
NIH ARDS Net FACTT- RESULTS
• PAC-guided therapy did not improve survival or organ function
• Associated with more complications than CVC-guided therapy
• Use of a conservative fluid management strategy in patients with ALI
• PAC should not be routinely used for themanagement of acute lung injury.
N Engl J Med 2006;354:2213-24.Critical Care 2008, 12:301
Practical guidelines for use of the pulmonary artery catheter
• Cardiac failure• Myocardial infarction complicated by
cardiogenic shock or progressive hypotension - class I indication ACC/AHA
• PAC insertion in AHF unnecessary, could be used to distinguish between a cardiogenic and a noncardiogenic mechanism in complex patients with concurrent cardiac and pulmonary disease- class IIb recommendation (level C evidence)
Critical Care 2006, 10(Suppl 3):S7
Eur Heart J 2005, 26:384-416.
Practical guidelines for use of the pulmonary artery catheter
Severe sepsis or septic shock• Guidelines do not recommend the routine use of
the PAC in shock Level 1(A)
• Monitoring combined with fluid infusion titrated to a goal-directed level of filling pressure associated with greatest increase in cardiac output and stroke volume
• PA occlusion pressure in the 12-15 mmHg range
Crit Care Med 2004, 32:1928-1948
Intensive Care Med. 2007;33:575–590 International Consensus Conference
Limitation of PAC monitoring
• Cost• Incorrect measurement of data
– calibration, damping, zeroing– transient respiratory muscle activity– reliance on digital readout– failure to wedge– non zone-III region
Limitation of PAC monitoring
• Incorrect interpretation of data– ventricular compliance– valve disease
• Improper therapeutic strategies - poor application of data on over zealous goals/targets
Mixed venous oxygen saturation (SvO2)
• SvO2 promoted as an indicator of changes in CO - Normal values for SvO2 - 70 to 75%
• Exercise, anemia, hypoxemia, and decreased cardiac output all decrease SvO2
• Hyperdynamic sepsis, hypothermia and muscle relaxation increase SvO2
• SvO2 above 70% does not reflect adequate tissue oxygenation ; persistently low SvO2 (< 50 %) is associated with tissue ischemia
Curr Opin Crit Care.2007; 13:318–323.
Central Venous Oxygen Saturation (ScvO2)
• Simple method to assess adequacy of global oxygen supply in various clinical setting
• Rivers et al - severe sepsis and septic shock-ScvO2 >70% / SVO2 > 65% absolute reduction of mortality by 15%(30.5 vs. 46.5%; p < 0.009) and major improvements in organ function - Level 1B
• ScvO2 tracks SvO2 except GA, severe head injury, redistribution of blood flow in shock,microcirculatory shunting or cell death
N Engl J Med.2001. 345:1368–1377Intensive Care Med. 2007;33:575–590 International ConsensusConference
Oxygen delivery (DO2) and consumption (VO2)
• Among various haemodynamic variables VO2 below required level most strongly related to death
• Oxygen consumption (VO2) = CO x Hb x (SaO2-SvO2) x 13.4 = 110-160 ml/min/m2
• Oxygen delivery (DO2) = CO x Hb x SaO2 x 13.4 = 520- 600 ml/min/m2
• Oxygen extraction (O2ER) = VO2/DO2 = (SaO2-SvO2) / SaO2 = 0.2 - 0.3
Critical Care 2006, 10(Suppl 3):S4
VO2 – DO2 interrelation
VO2 = DO2 x OER
VO2
DO2
Critical DO2
Maximal OER NORMAL VO2 becomes
supply dependent
SHOCK
Clinical implications• The Supranormal DO2 Approach
• Shoemaker : DO2 maintained supranormal values (at least 600 ml/min.M²) in all patients at risk of complications, to ensure sufficient oxygen availability Chest. 1988; 94:1176–1186
• Guidelines do not recommend targeting supranormal oxygen delivery in patients with shock Level 1A
• The Titrated Approach• individualized according to careful clinical
evaluation, cardiac index, SvO2, blood lactate concentrations Intensive Care Med. 2007;33:575–590
International Consensus Conference
Blood Lactate Levels • Sepsis is accompanied
by hypermetabolic state, with enhanced glycolysis and hyperlactataemia -not due to hypoxia
• Marker of tissue perfusion and adequacy of resuscitation
• Blood lactate concentration in excess of 4 mmol /L: is associated with a high risk of mortality
Curr Opin Crit Care.2006 12:315–321
Clinical Implications • Appropriate to use elevated lactate trigger to initiate
aggressive care- Level 1C• In the event of hypotension and/or lactate > 4 mmol/l
(36 mg/dl):– initial minimum of 20 ml/kg of crystalloid (or colloid
equivalent)– Apply vasopressors for hypotension not responding
to initial fluid resuscitation to maintain MAP >65 mmHg
• In the event of persistent hypotension despite fluid resuscitation (septic shock) and/or lactate > 4 mmol/l (36 mg/dl):– Achieve central venous pressure > 8 mmHg– Achieve central venous oxygen saturation >70%
Surviving Sepsis Campaign.2008
Conclusions • A knowledge deficit disorder continues to
exist in ICU regarding ideal hemodynamic monitoring
• Major problem is the user not the device of monitoring
• RCTs in homogenous populations are necessary.
• Tx must be rigorously protocolized as per monitoring in order to have a positive outcome